Hirotaka Sugiura

Vanderbilt University, Nashville, MI, United States

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Publications (17)46.87 Total impact

  • [show abstract] [hide abstract]
    ABSTRACT: Suppression of implantable defibrillator discharges associated with ventricular tachyarrhythmia (VTA) has been reported for sotalol. This study aimed to investigate the efficacy of intravenous nifekalant hydrochloride in predicting the effects of oral sotalol. The present study included 14 patients who had sustained VTA associated with structural heart disease. All patients also had inducible VTA. To compare the effects of nifekalant and sotalol, programmed electrical stimulation was performed, in the basal state, after nifekalant administration, and after sotalol administration. Nifekalant and sotalol similarly prolonged the corrected QT interval and ventricular effective refractory periods, but the heart rate was slowed by sotalol only. In 4 of 5 patients whose VTA became non-inducible by nifekalant, subsequent treatment with sotalol also suppressed the inducible VTA. In all of the 9 patients non-responding to nifekalant, VTA remained inducible during sotalol treatment. Nifekalant accurately predicted the response to sotalol during electrophysiologic study in 13 of 14 patients. Of 11 patients who remained on sotalol, VTA recurred in 3 non-responders during a follow-up of 46 +/- 11 months. Nifekalant and sotalol had similar effects on inducible VTA. The response of inducible VTA to nifekalant may predict the clinical efficacy of sotalol.
    Circulation Journal 06/2006; 70(5):583-7. · 3.58 Impact Factor
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    ABSTRACT: This study investigated the treatment of ventricular tachycardia (VT) after repair of tetralogy of Fallot or double outlet of the right ventricle. The ideal antiarrhythmic therapy for VT in patients after repair of congenital heart disease, especially without left ventricular dysfunction, has not yet been established. Seven consecutive patients (2 women and 5 men) with stable monomorphic sustained VT were investigated. The mean age was 25 +/- 7 years (range, 16-35 years). Four patients had undergone surgical repair of tetralogy of Fallot, and 3 had surgical correction of double outlet of the right ventricle at the mean age of 18 +/- 7 years (range, 9-27 years) before documentation of the arrhythmia. The mean ejection fraction of the left ventricle was 60% +/- 8% (range, 50-72). Fourteen sustained monomorphic VTs were induced in 7 patients using programmed electrical stimulation. The mean cycle length of tachycardia was 346 +/- 77 milliseconds (range, 260-480 seconds). The site of the surgical correction of the right ventricle was associated with the origin of VT in all patients. Radiofrequency catheter ablation was attempted in 8 VTs in 7 patients: 7 clinical and 1 nonclinical VTs. In 6 patients, class III antarrhythmic agents were added because VT remained inducible after ablation. During a follow-up of 61 +/- 29 months (range, 15-110 months), there were no recurrences of VT. In patients with drug-refractory VT originating from the right ventricle late after congenital heart disease, and when their left ventricular function do not deteriorate, combined therapy for radiofrequency catheter ablation with class III antiarrhythmic agents might effective and should be considered as a therapeutic option.
    Journal of Electrocardiology 05/2006; 39(2):219-24. · 1.09 Impact Factor
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    ABSTRACT: Some patients with an implantable cardioverter-defibrillator (ICD) suffer from burst of inappropriate multiple discharges (severe electrical storm), and because the current therapeutic options are limited, the effect of nifekalant hydrochloride, a new class III drug, on severe electrical storm was investigated in the present study. Ninety-one consecutive patients treated with ICD were included in the study (M 70; mean age 58 years; left ventricular ejection fraction 45+/-15%). Severe electrical storm was defined as more than 10 ICD discharges within 1 h. During a mean follow-up period of 30+/-13 months, 41/91 (45%) patients had appropriate ICD therapy for arrhythmias and severe electrical storm occurred in 11 of them (12%) at 20+/-18 months after ICD implantation. The mean number of ICD discharges/h during severe electrical storm was 18+/-12. In 4 of 10 patients, severe electrical storm was successfully suppressed by a combination of deep sedation and beta-blocking agent; 6 other patients were refractory to this treatment, but severe electrical storm was successfully suppressed by intravenous administration of nifekalant hydrochloride with no adverse effects. Nifekalant hydrochloride is an effective and safe treatment for severe electrical storm.
    Circulation Journal 01/2006; 69(12):1508-13. · 3.58 Impact Factor
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    ABSTRACT: Electrical abnormalities in the RVOT may be involved in Brugada syndrome. We investigated the relationship between the signal-averaged ECG (SAECG) and electrophysiologic study (EPS), especially focusing on conduction delay in the outflow tract of the right ventricle (RVOT) and its contribution to clinical characteristics. Twenty-four patients with Brugada syndrome (23 men and 1 woman; 61 +/- 16 years old) were studied. We assessed the presence of late potential (LP) in SAECG and the filtered QRS duration in the right precordial leads (V1 or V2; RfQRS) and in the left precordial leads (V5 or V6; LfQRS) and the difference between them. In 18 patients, SAECG was evaluated for an LP on three separate occasions. SAECG was positive for LP in 15 patients at least once; and in 7 patients, SAECG was positive for an LP on multiple occasions, and 6 of 7 patients (86%) had a history of cardiac arrest. The difference between RfQRS and LfQRS was significantly greater in patients with cardiac arrest than in patients with syncope or in asymptomatic patients; 29 +/- 10, 14 +/- 11 (P < 0.01), and 7 +/- 5 msec (P < 0.001), respectively. All patients were alive and one patient with cardiac arrest had an appropriate VF therapy delivered by the ICD. The dominant prolongation of the filtered QRS duration in the right precordial leads may be related to the risk of arrhythmic event in Brugada syndrome.
    Journal of Cardiovascular Electrophysiology 12/2005; 16(12):1311-7. · 3.48 Impact Factor
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    ABSTRACT: Disopyramide is thought to have an advantageous effect for atrial fibrillation (AF) associated with vagal activity because of its anticholinergic effect. We used a canine vagal nerve stimulation (VNS) model. The monophasic action potential (MAP) duration at 90% repolarization (MAP(90)), the intraatrial conduction time, the induciblity of AF by electrical stimulation, and the amplitude of high-frequency component (HF-amp) of the heart rate variability (HRV) were evaluated before and after the administration of disopyramide (1 mg/kg) (group D, n = 8) or pilsicainide (1 mg/kg) (group P, n = 5). In group D, HF-amp decreased in the baseline condition from 1.1 +/- 0.6 to 0.6 +/- 0.4 ms and the degree of VNS-induced augmentation of HF-amp was attenuated from +492% to +127%. VNS-induced shortening of MAP(90) was also attenuated in the right atrium (from -30 +/- 15% to -10 +/- 6%) and in the left atrium (from -15 +/- 9% to -6 +/- 6%). In group P, little effect was shown in these parameters. The vagotonic AF became noninducible in all eight experiments in group D, while in only one of five in group P. The beneficial effect of disopyramide for vagotonic AF is based on the decrease of basal vagal tone and attenuation of the effect of vagal stimulation in the atrial myocardium. HRV is a useful parameter for evaluation of the effect of antiarrhythmic drugs on the autonomic nerve system, and the evaluation of variability may be useful for testing drug efficacy for arrhythmias.
    Pacing and Clinical Electrophysiology 12/2005; 28(11):1208-14. · 1.75 Impact Factor
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    ABSTRACT: We describe here the case of a 58-year-old female patient who experienced inappropriate shocks from her implantable cardioverter-defibrillator (ICD). Stored electrograms from her ICD showed high frequency noise preceding the shock. Although the pacing threshold was normal and lead fracture was not found in chest X-rays, pacing lead impedance decreased to 480 omega. Moreover, such high frequency noise was observed by electrogram telemetry, but not by routine evaluation every 3 months. ICD lead dysfunction was suspected, so we elected to replace the ICD lead system. At the time of the operation, lead impedance was 410 omega and pacing threshold was the same as it was at the time of the ICD implantation, and no lead insulation disturbances were observed in the generator pocket. However, manipulation of the lead system produced high frequency noise reproducibly. Since some of the ICD lead dysfunction initially was clinically silent at rest, dysfunction was difficult to detect before serious problems occurred. Therefore, more careful evaluation of the ICD lead system is needed during long-term follow-up of ICD implants.
    International Heart Journal 10/2005; 46(5):909-13. · 1.23 Impact Factor
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    ABSTRACT: This study was performed to clarify the antiarrhythmic effects of magnesium sulfate (Mg(++)) in a prolonged QT interval canine model of polymorphic ventricular tachyarrhythmia (VTA). In six experiments in a canine model of prolonged QT by anthopleurin-A, Mg(++) was administered in boluses of 0.2 mL/kg during repetitive episodes of self-terminating polymorphic VTA or frequent premature ventricular complexes (PVCs). The distribution of ventricular repolarization across the left ventricular(LV) wall and dispersion of transmural repolarization were analyzed before, and 30 and 120 seconds after Mg(++) administration, during ventricular pacing at 100 bpm. Transmural unipolar electrograms were recorded from multipolar needle electrodes, and local activation-recovery intervals (ARI) were measured. Mg(++) rapidly eliminated self-terminating polymorphic VTA and all isolated PVCs. During ventricular pacing at 100 bpm, Mg(++) caused modest shortening of ARI at all recording sites. Since the magnitude of ARI shortening was greater at mid-myocardial sites than at other ventricular sites, mean transmural ARI dispersion decreased from 80 +/- 22 to 45 +/- 18 ms within 30 seconds after Mg(++) injection. However, this effect was transient, and, at 120 seconds after Mg(++) administration, ARI had increased all sites and transmural ARI dispersion lengthened to 65 +/- 18 ms. Besides suppression of triggered premature activity, homogenization of transmural ventricular repolarization was associated with the antiarrhythmic effects of intravenous Mg(++) in this model. Since these effects were transient, a continuous intravenous infusion of Mg(++) is preferred to prevent recurrences of VTA.
    Pacing and Clinical Electrophysiology 09/2005; 28(8):844-50. · 1.75 Impact Factor
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    ABSTRACT: Quinidine, a class I antiarrhythmic agent with blocking property of transient outward current, is a possible candidate for the suppression of ventricular fibrillation in patients with Brugada syndrome; although there is a concern that its ability to these effects may be proarrhythmic. Therefore, we evaluated the effect of quinidine sulfate on ST-segment elevation in Brugada syndrome. In 8 patients with Brugada syndrome, the magnitude of ST-elevation at the J-point (ST(J)), and the ST-segment configuration in leads V1-V3, were compared before and on day 2 after the initiation of quinidine administration. In 3 patients, quinidine attenuated ST(J) by > or = 0.1 mV. Of these 3 patients, ST-segment elevation was normalized in 2 patients, while the ST-segment configuration was unchanged in another. In another 3 patients, quinidine augmented ST(J) by > or = 0.1 mV without any change of ST-segment configuration, and the augmentation was returned to baseline after the discontinuation of quinidine. Quinidine exhibited no effect on the ST-segment in the remaining 2 patients. The favorable effects of quinidine on the ST-segment tended to be more pronounced in patients with prominent ST-elevation at baseline. In 1 patient, quinidine was effective in eliminating both ST-segment elevation and repetitive tachyarrhythmia episodes. In conclusion, the effects of quinidine on ST-segment elevation were variable. Quinidine may potentially augment the ST-segment elevation in some patients with Brugada syndrome.
    Pacing and Clinical Electrophysiology 05/2005; 28(5):372-7. · 1.75 Impact Factor
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    ABSTRACT: The aim of this study was to investigate the long-term efficacy and safety of electrophysiologic study (EPS)-guided sotalol administration combined with implantable cardioverter defibrillators (ICD) for ventricular tachyarrhythmias (VTA). This study enrolled 92 patients with both structural heart disease and sustained VTA. Sotalol was administered to 57 patients, and its efficacy was assessed by EPS. Long-term treatment was continued in combination with ICD in 31 patients (57%) whose VTA was no longer inducible (responder group) and in 16 patients whose VTA remained inducible (nonresponder group). The long-term outcomes were compared among the responder group, the nonresponder group, and 35 ICD recipients untreated with antiarrhythmic drugs (ICD-only group). During a mean follow-up of 44 +/- 33 months, the recurrence of VTA was not significantly different between all patients treated with sotalol (30%) and patients in the ICD-only group (46%). However, the recurrence of VTA was significantly lower in the responder (13%) than in the nonresponder (63%) or the ICD-only groups (46%). There was no significant difference in VTA recurrence between the nonresponder and the ICD-only groups. One patient each in the responder and the ICD-only groups died suddenly, and all-cause mortality was similar in the three groups. The incidence of inappropriate ICD discharges was less in the sotalol than in the ICD-only groups. No patient had to discontinue long-term sotalol treatment because of the adverse effects. In conclusion, sotalol reduced VTA recurrence in the responding patients and inappropriate ICD discharge. EPS may predict the efficacy of sotalol for VTA recurrence.
    Pacing and Clinical Electrophysiology 05/2005; 28(4):285-90. · 1.75 Impact Factor
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    ABSTRACT: In patients with Brugada syndrome, implantable cardioverter defibrillator (ICD) is the only reliable treatment to prevent sudden death though, in some cases, internal defibrillation may be unsuccessful. The aim of this study was to examine the determinants of defibrillation failure, with a focus on electrophysiologic characteristics. The study included 51 patients treated with ICD: 22 with Brugada syndrome and 29 with structural heart disease (SHD). The prevalence of defibrillation energy requirement precluding the programming of a 10-J safety margin, the mean right ventricular effective refractory period (ERP), and mean induced ventricular fibrillation cycle length (VFCL) from the stored ICD electrograms, were compared between the two patient groups. High defibrillation requirements were observed in 18% of patients with Brugada syndrome versus 0% of patients with SHD. However, the patients with SHD had larger heart size than those with Brugada syndrome. Mean VFCL and mean ERP were both significantly shorter in patients with Brugada syndrome than in patients with SHD, and ERP and VFCL were significantly correlated. Patients with Brugada syndrome have a high prevalence of high defibrillation energy requirement, and short ventricular ERP and VFCL.
    Journal of Cardiovascular Electrophysiology 04/2005; 16(3):262-6. · 3.48 Impact Factor
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    ABSTRACT: A 74-year-old man with a history of partial gastrectomy presented with an electrocardiogram consistent with Brugada syndrome and marked meal related fluctuations in the ST segment. ST-segment elevation was prominently attenuated at 30 minutes and increased at 120 minutes after meals. Analysis of heart rate variability revealed a relationship between postprandial heightened parasympathetic activity and increase in Brugada-type ECG abnormality. A rapid postprandial increase in blood glucose may initially stimulate sympathetic nervous activity and secondarily increase parasympathetic tone. Food intake can be associated with fluctuations in ST-segment elevation in patients with the Brugada syndrome.
    Pacing and Clinical Electrophysiology 12/2004; 27(11):1560-2. · 1.75 Impact Factor
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    ABSTRACT: A 30-year-old man was admitted for treatment of tachycardia-induced cardiomyopathy caused by incessant atrioventricular nodal reentrant tachycardia (AVNRT). An echocardiogram revealed dilatation of all cardiac chambers with severe globally depressed biventricular systolic function. During an electrophysiologic study, HV interval was prolonged to 118 ms by atrial extrastimulus and 2:1 HV block was documented during AVNRT. Four weeks after catheter ablation for AVNRT, an echocardiogram demonstrated regression of the wall motion abnormality of both ventricles and of their dimensions. In the electrophysiologic study, the HV conduction disturbance disappeared. So far, this is the first case in which tachycardia-induced cardiomyopathy was accompanied by transient His-Purkinje conduction abnormality.
    Journal of Electrocardiology 11/2004; 37(4):315-9. · 1.09 Impact Factor
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    ABSTRACT: Cardiac sarcoidosis is increasingly recognized and is associated with poor prognosis. Ventricular tachycardia (VT) associated with cardiac sarcoidosis is the most likely cause of sudden death in most patients, but the mechanism has not been well established. This study investigated the mechanisms and outcome of VT associated with cardiac sarcoidosis. The study included eight consecutive patients (five men, three women, aged 54 +/- 19 years) who had sustained monomorphic VT associated with cardiac sarcoidosis in our hospital. The average ejection fraction was 43 +/- 11%. Twenty-two VTs were observed in these patients, and mean heart rate during VT was 192 +/- 29 beats/min (range 144-259). The phenomenon of transient entrainment was documented in 10 of 22 (45%) VTs by ventricular pacing (eight in the active phase). Another five (23%) VTs could not be entrained, but could be initiated by programmed stimulation and terminated by rapid pacing, reproducibly. In 3 of the 22 (14%) VTs, cardioversion was required urgently because of the fast rate, while the remaining 4 (18%) could be induced during electrophysiologic study. In this study, there was a high possibility that the mechanism of 15 (68%) VTs was reentry. Reentrant substrate is formed not only in association with the healing of cardiac granulomas in the inactive phase of cardiac sarcoidosis but also in the active phase. Ventricular tachycardia with cardiac sarcoidosis, even if this mechanism is reentry, has different inducibility between the active and inactive phases in an electrophysiologic study. This makes the therapy for cardiac sarcoidosis (e.g., corticosteroids, antiarrhythmic agents, and catheter ablation) difficult. The implantable cardioverter-defibrillator is an effective treatment for ventricular tachyarrythmia with cardiac sarcoidosis.
    Clinical Cardiology 05/2004; 27(4):217-22. · 1.83 Impact Factor
  • Circulation 02/2004; 109(2):277. · 15.20 Impact Factor
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    ABSTRACT: The ventricular tachyarrhythmias associated with the LQT3 syndrome are typically bradycardia-dependent. However, some episodes can be associated with exercise or emotional stress, suggesting a different arrhythmogenic mechanism when sympathetic activity predominates. This study examined the potential arrhythmogenic mechanisms during periods of autonomically mediated transient heart rate acceleration in a canine anthopleurin-A model of LQT3 syndrome. Using plunge needle electrodes, transmural unipolar electrograms of the left ventricle were recorded from endocardial (Endo), mid-myocardial (Mid) and epicardial (Epi) sites. The activation-recovery interval (ARI) was measured to estimate local refractoriness. The cardiac cycle length was gradually shortened by cessation of vagal stimulation (vagal stimulation protocol (VSP)), and intramural electrograms and onset mode of ventricular tachyarrhythmias were analyzed in 7 experiments. The VSP was performed 8 times before and 5 times after administration of mexiletine in each experiment. Before mexiletine, vagal stimulation slowed the heart rate and created large transmural ARI dispersion because of a greater ARI prolongation at Mid rather than Epi/Endo sites. After cessation of vagal stimulation, unipolar electrograms started to show ARI alternans and ventricular premature beats developed sporadically. Sustained ventricular tachyarrhythmias were induced in 12 of the 56 trials of the VSP. Initiation of ventricular tachyarrhythmias was associated with delayed conduction at Mid/Endo sites. Mexiletine attenuated transmural ARI dispersion, and neither ARI alternans nor ventricular tachyarrhythmias was observed during all 35 trials of the VSP after mexiletine administration. Heart rate acceleration induced by an abrupt shift to a state of predominant sympathetic activity enhances arrhythmias in this LQT3 model. Mexiletine homogenizes ventricular repolarization, suppresses premature complexes and was antiarrhythmic during ventricular tachyarrhythmias induced by the VSP.
    Circulation Journal 04/2003; 67(3):263-8. · 3.58 Impact Factor
  • Circulation Journal - CIRC J. 01/2003; 67(3):263-268.
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    ABSTRACT: Aims: In selecting effective antiarrhythmic agents for reentrant ventricular tachycardia (VT), there is no hallmark which can predict drug-efficacy. In this study, the ability of dl-sotalol to suppress the inducible VT was assessed during an electrophysiologic study with special reference to the zone of entrainment, an index of the excitable gap. Methods and Results: In 21 patients, monomorphic sustained VT was induced and entrained with rapid ventricular pacing at progressively shorter cycle lengths until VT was terminated at a critical length (=block cycle length) and the width of the zone of entrainment was calculated as the difference between the cycle length of VT and the VT-interrupting critical cycle length: the longest cycle length at which 1:1 conduction fails within the zone of slow conduction. The effective refractory period was measured by extrastimulus technique. After the administration of dlsotalol (240-320mg/day for>14 days), the drug efficacy was evaluated by an electrophysiologic study and the relation to the basal electrophysiological parameters were analyzed. After the administration of dl-sotalol, the cycle length of the sinus rate, the QT interval, and the effective refractory period were prolonged significantly. In 11 patients, VT was not induced (responders) to the end of the entire protocol of induction. In another 10 patients, dl-sotalol proved a failure and a slower VT with a similar width of zone of entrainment remained inducible. The cycle length of VT and the width of the zone of entrainment did not differ between the responders and non-responders to dl-sotalol: 300±72 vs. 275±21 msec and 57±27 vs. 50±16 msec, respectively. Conclusions: The VT induction was prevented by dl-sotalol in 52%, but the cycle length, the zone of entrainment of VT, and other variables were not different between the responders and non-responders to dl-sotalol.
    01/2003;

Publication Stats

107 Citations
702 Views
46.87 Total Impact Points

Institutions

  • 2006
    • Vanderbilt University
      • Division of Clinical Pharmacology
      Nashville, MI, United States
  • 2003–2006
    • Niigata University
      • • Department of Internal Medicine
      • • Division of Cardiology
      • • School of Health Sciences
      Niahi-niigata, Niigata, Japan